Fatty15
Masters of Marketing Disguised as Science
This presentation reflects the personal opinions of the speaker, based on publicly available information as of September 13, 2025. It is intended as commentary and critique for educational purposes only. The content does not provide medical advice. No affiliation with, or endorsement by, Fatty15 or related entities is intended or implied.
Fatty15: Better than Everything
“100+ peer-reviewed studies have been published by independent scientists throughout the world on the benefits of C15:0, including the pure C15:0 ingredient in fatty15.”
“C15:0 is emerging as the first essential fatty acid to be discovered in over 90 years.”
“C15:0 is a pleiotropic nutrient with multiple dose-dependent mechanisms of action.”
“An estimated 1 in 3 people may have Cellular Fragility Syndrome.”
“Fatty15 fixes C15:0 deficiencies & reverses Cellular Fragility Syndrome”
“Clinical Trial Results: Fatty15 Can Treat Nutritional C15:0 Deficiencies”
“lower inflammation, and repair mitochondrial function”
“C15:0 helps support and balance mood”
“C15:0 helps support healthy cells by targeting key hallmarks of aging”
“helps support your metabolism and healthy weight on a cellular level”
“The Longevity Nutrient” “fatty15 has emerged as a leading longevity-extending geroprotector”
Essential
Essential Fatty Acid
“could it be essential?”; 2020 Study
“is emerging as an essential fatty acid”; 2022 Study
“(C15:0) is an essential odd-chain saturated fatty acid”; 2023 Study
“essential”, “newly identified nutritional C15:0 deficiency syndrome (“Cellular Fragility Syndrome”)“; 2024 Study
“emerged as…essential…required by animals to support both early development and long-term health”, “supporting cognitive health”; 2025 Study
Every single author of all 5 of these studies is either a co-founder / equity holder / advisor / funded by / an employee of the company that makes and promotes fatty15.
(except one recurring research collaborator from the U.S. Navy Marine Mammal Program)
GRAS
GRAS (Generally Recognized as Safe)
- Our ingredient is officially GRAS (generally regarded as safe) certified, which means fatty15 is safe for pregnant women and nursing moms.
- In our commitment to make fatty15/FA15/C15:0 accessible to all, we have gone above and beyond to enforce the safety of fatty15 for those of all ages and life stages by receiving GRAS (Generally Recognized As Safe) status by the FDA.
No official “GRAS certification” from the FDA. “Certified” implies FDA approval.
- Two Ways to Achieve GRAS Status
- GRAS Notification program: Submit to FDA detailing ingredient. FDA evaluates. GRAS Database
- Self-affirmation: company itself assesses safety of an ingredient and declares it GRAS, without submitting anything to the FDA
“With a recent self-GRAS (Generally Recognized as Safe) affirmation” FA15 can now be used in food and beverage products.
“FA15™ has been approved as a food ingredient that can be used daily, up to 245 mg per day.”
Fatty15’s GRAS status is self-declared.
Not public. FDA has not reviewed or approved it.
Fatty15 > omega-3
Fatty15: 3x better than omega-3
Deep Dive: Fatty15 vs. Omega-3; The Science
“Simply put, fatty15 is better, broader and safer than the purest, highest performing omega-3 (EPA) in repairing and restoring cellular (aka your) health.”
“Fatty15 repairs 2.5x more cell types compared to omega-3.”
“Fatty15 had 36+ cellular benefits across 83% of cell types tested, which was 3x better than omega-3.”
- 100% in vitro (cell-based) study, by founder, unclear if relevant in humans.
- 3× better than omega-3?
- C15:0 showed 36 annotated, dose-dependent activities (ie at multiple doses)
- 12 activities were shared between C15:0 and EPA at 17 μM
- mixing a multi-dose C15:0 count with a single-dose overlap with EPA?
- Repairs 2.5× more cell types?
- C15:0…broad anti-inflammatory and anti-proliferative activities…across 10 systems (“repairs”)
- EPA at 50 μM was cytotoxic to 4 of the 12 cell systems
- 10 / 4 ? therefore 2.5x ?
Take Fatty15 instead of omega-3 / EPA
Note: This is a scientific/consumer-protection opinion, not medical advice or an allegation of unlawful conduct.
Unsupported substitution claim. There are no human or animal randomized trials showing C15:0 is superior to EPA/DHA on clinical outcomes; the “3×” claim comes from unreproducible math from a single company-affiliated in-vitro screen rather than outcome trials.
fatty15 “3×” marketing, PLOS ONE in-vitro paper + competing-interest statementContrary to major guideline recommendations. Major authorities advise obtaining EPA/DHA because ALA conversion is limited and fish intake (or Rx EPA) lowers risk in specific populations; telling consumers to replace omega-3s runs counter to that guidance.
NIH ODS Omega-3 fact sheet, AHA fish/EPA-DHA guidancePotential for consumer harm. Substitution could dissuade people, especially higher-risk patients, from nutrients and therapies with outcome data (e.g., icosapent ethyl reduces CV events when added to statins). NEJM REDUCE-IT trial, FDA label icosapent ethyl
Essential nutrient substitution risk. Omega-3 fatty acids (ALA, with EPA/DHA in practice) are essential nutrients with unique roles in neurodevelopment, vision, cardiometabolic health, and mental health. Promoting C15:0 as a replacement implies it can substitute for these essential functions, which is unsupported and potentially harmful, especially for developing children and pregnant women.
NIH ODS Omega-3, Omega-3s and mental health review (NIH/PMC)Inadequate substantiation for a comparative health claim. Under FTC standards, comparative efficacy claims require “competent and reliable scientific evidence”, typically well-controlled human studies. An in-vitro screen doesn’t meet that bar.
FTC Health Products Compliance GuidanceConflicts of interest / non-independence. The in-vitro “3×” paper is authored by company-affiliated inventors with licensed patents; it is not independent and has not been replicated in clinical trials. PLOS ONE competing-interest statement
Over-extrapolation from cell assays. Cell-panel biomarker differences ≠ clinical benefits in people; dose/exposure relevance and translation are unproven for the claimed endpoints. PLOS ONE methods/limitations
Irreplaceable role. Essential = only that nutrient (or its specific obligate precursor) suffices to prevent deficiency. Fatty15 cannot replace ALA, an essential fatty acid, precursor to omega-3
- This analysis reflects my opinions based on the publicly cited sources and the state of evidence as of September 13, 2025. It is offered for informational and public-interest commentary only. It is not medical or legal advice, and it is not a statement of fact about any company’s intent, ethics, or lawfulness. I do not allege wrongdoing and welcome corrections or additional independent evidence. I have no financial relationship with the products or companies discussed. All trademarks are the property of their respective owners.
In my view: promoting C15 as substitute for omega-3 is borderline unethical.
Decades of omega-3 research vs. one founder-run cell study.
Fatty15 and RCTs
Is Fatty15 Legit
“Is Fatty15 Legit” Series: Are there clinical trials supporting C15:0 & fatty15 benefits?
“If you’re here, chances are that you recently heard about fatty15, a healthy aging supplement containing C15:0. And you may be wanting to know if this supplement is legit.”
“Are there clinical trials supporting C15:0 & fatty15 benefits?”
“Yes, there are a growing number of clinical trials supporting C15:0 and fatty15’s health benefits.
Here’s a breakdown of the six clinical trials and seven studies to date:”
Clinical Trial 1
“Stallings et al. led a clinical trial with healthy humans to determine the oral bioavailability and pharmacokinetics of pure C15:0, the same ingredient provided in fatty15.”
“Participants were provided a single oral dose of C15:0 and showed that circulating C15:0 levels reliably increased.
For every 100 mg of ingested pure free fatty acid C15:0, C15:0 circulating levels increased on average by 1 ug/ml.”
Clinical Trial 2
“Mascarenhas et al. then led a clinical trial…to extensively model the oral bioavailability and pharmacokinetics of pure C15:0”
“…repeated findings from the Stallings et al. study. Namely, that
for every 100 mg of ingested pure free fatty acid C15:0, circulating C15:0 levels increased on average by 1 ug/ml.”
“The authors concluded that pure free fatty acid C15:0 is, on average, 100% bioavailable.”
Clinical Trial 4
88 Chinese females with NAFLD were randomly assigned to 1 of the 3 groups for 12 wk: diet with 300mg daily C15:0 supplementation (n = 31), diet without C15:0 supplementation (n = 28), or control (habitual diet and no C15:0 supplementation, n = 29). Treatment diet was Asian-adapted Mediterranean diet.
“While all three groups had lowered liver fat and body weight loss, the C15:0 supplemented group trended to having the greatest loss of liver fat and body fat. It is important to note, however, that these shared improvements among all three groups were not statistically significantly between the groups.”
“The authors conclude that C15:0 supplementation had early evidence of providing clinically relevant benefits related to lower LDL cholesterol and an improved gut microbiome.”
Clinical Trial 4
List of Metrics unchanged with addition of 300mg daily C15:
Body weight, BMI, Total fat mass, Fat-free mass, Waist circumference,
Visceral adipose tissue (VAT) volume, Subcutaneous abdominal adipose tissue (SAT) volume, Superficial subcutaneous abdominal adipose tissue (SAT), Deep SAT,
Liver fat (MRI-PDFF), Controlled Attenuation Parameter (CAP) score, Intramyocellular lipid (soleus IMCL/water), Pancreatic fat PDFF (head–body), Pancreatic fat PDFF (tail),
Systolic blood pressure, Diastolic blood pressure, Fasting glucose, Fasting insulin, HOMA-IR, HbA1c, Total cholesterol, HDL-cholesterol, Triglycerides,
Gamma-glutamyl transferase (GGT), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Alkaline phosphatase (ALP), C-reactive protein (CRP), Resting metabolic rate (RMR), Physical activity (steps/day),
Sleep duration, STAI—State anxiety score, STAI—Trait anxiety score, BDI-II depression score,
Note: ignoring microbiome results
Total Metrics measured: 35
Metrics unchanged with C15: 34
Metrics changed with C15: 1
*it did on average increase C15 levels
Clinical Trial 5
Not a separate clinical trial. Additional data analysis of Trial 4.
“This post-hoc analysis showed that, while all three groups had lower body weight and improved mood, the C15:0 supplemented group had the most significant improvement in mood.
“The authors conclude that C15:0 supplementation may have a positive effect on improving mood.”
Study quotes:
- “The present study cannot conclude that the group receiving C+15:0 together with the MD had effects in decreasing symptoms.”
- “These findings suggest that both dietary interventions had comparable effects on anxiety and depression within the study population.”
Clinical Trial 6
Not on Fatty15 or C15:0 supplementation. It’s on high or moderate dairy fat diets. Much less relevant.
“Clinical Trial 6: Arghavani et al. led a cross-over clinical trial that included healthy adults to evaluate the potential effects of dairy fat diets, as well as individual fatty acid components within dairy fat, on blood pressure and vascular stiffness”. “This clinical trial showed the following:”
The 2025 paper by Arghavani et al. is a secondary analysis of data from an already‐conducted randomized crossover trial.
There is nothing in the original RCT about C15.
Original RCT - “Objective: The aim of this clinical trial was to evaluate the impact of high dairy product intake (HD) (≥4 servings/d) for 6 wk, compared with an adequate dairy product intake (AD) (≤2 servings/d), on glycemic and insulinemic parameters, insulin sensitivity, insulin secretion, and β-cell function in hyperinsulinemic adults.”
Clinical Trial 7
“Kaneko et al. led a randomized, placebo-controlled clinical trial that included older women to evaluate the potential effects of an oral high-C15 algal oil on skin elasticity, collagen density, and skin moisture. This clinical trial showed that daily oral intake of high-C15 algal oil for 12 weeks improved skin elasticity, collagen density, and skin moisture.”
“The authors conclude that oral intake of high C15-containing supplements provides skin health benefits.”
Orlan oil, containing C:15 but also many other fatty acids like DHA, DPA, EPA.
Dose of C15 per day: ~9mg
Summary so far
Of the 6 “clinical trials supporting C15:0 or fatty15 benefits”:
- Trials 1 and 2 are validating a fat malabsorption test.
- Trial 4: C15 doesn’t appear to help NAFLD (even at higher dose than fatty15 recommends).
- Trial 5 is a secondary analysis of Trial 4; authors “cannot conclude” added benefit of C15:0.
- Trial 6 is not on C15 supplementation and is not a trial.
- Trial 7 C15 daily dose contains only 9mg; oil blend containing DHA, DPA, EPA.
- All 6 are not on actual fatty15.
- Mis/Overstatements about what the cited study actually did/found.
- Robust evidence it does anything beneficial? Not supported.
Only one actual RCT on C15 supplementation.
Outcomes were almost entirely diet/weight-loss–driven
(minor LDL drop with C15).
Clinical Trial 3
Clinical Trial 3
The only RCT in humans on actual on Fatty15.
- Study design: double-blind, randomized, placebo-controlled, 2-arm trial.
- Population: 30 young adults (ages 18–25) with overweight or obesity
- Intervention: 200 mg of C15:0 (fatty15) daily vs. placebo for 12 weeks.
- Randomization: 20 participants assigned to C15:0 supplementation and 10 to placebo
- Primary outcome: change in plasma C15:0 concentration.
- Secondary outcomes: safety, tolerability, and exploratory measures (e.g., liver enzymes, hemoglobin, glucose, cholesterol).
Conclusions
- C15:0 supplementation significantly increased plasma C15:0 by 1.88 μg/mL compared to placebo.
- Treatment was safe and well tolerated.
- Main secondary analysis: GGT increased by ~10 U/L in placebo but decreased by ~1 U/L in treatment, giving a significant between-group difference of ~11 U/L (interpret cautiously)
- In subgroup analysis of the secondary outcomes:
- “significantly greater decreases in ALT (-29 U/L, P = 0.001) and AST (-6 U/L, P = 0.014), as well as a greater increase in hemoglobin (0.60 g/dL, P = 0.010), as compared with participants that did not reach a posttreatment level >5 μg/mL”
Clinical Trial 3
Subgroup analysis of the secondary outcomes:
Half (10) of the treatment group did not achieve C15 blood levels of > 5 μg/mL
Authors state: “Given the inter-individual variance in treatment response, a nuanced appraisal relative to a proposed threshold of 5 μg/mL was pursued.”
based on end-of-treatment plasma C15:0 levels
“informed by epidemiological and preclinical literature”
after the fact, non-randomized, exploratory subgroup analysis
“Among participants who adhered to the protocol, their C15:0 levels increased at the same amounts demonstrated by Mascarenhas et al. and Stallings et al.
Namely, 200 mg of C15:0 resulted in raised circulating C15:0 levels of 2.3 ug/ml.” - fatty15
Change in plasma C15:0 levels
- 7 participants in treatment group were already above 5 μg/mL at baseline
- nobody in treatment group went from above to below threshold
- 4 in Placebo group were from above to below threshold
- Adherence per group:
- 95% Threshold group (171 total pills)
- 84.3% Sub-threshold group (152 total pills)
- 10 in treatment, despite taking on average 84.3% (152) of pills did not cross threshold
C15:0 Plasma Level Increase
“C15:0 levels increased among participants who strictly adhered to the protocol.”
Reverse logic: Groups were formed after the study, based on final C15:0 levels, not on adherence.
- Trial can’t establish a general rule that “the more total supplementation taken, the higher the levels.”
- This was not tested in the study. There was no dose-response analysis.
- Study never states adherence explained 80% of difference. Unclear where this value comes from.
- “nutritionally sufficient threshold” language was not used in the study is not an externally validated standard.
Study states: the adherence–response link was “not strong enough to explain the response heterogeneity alone”
“This study was not designed or powered to expound further on this observation, and future studies will need to address these discrepancies.”
Liver Function in Threshold Group
“Among participants who adhered to the protocol, their C15:0 levels increased…This group with raised C15:0 levels also had significantly improved liver function (lower ALT and AST), as well as raised hemoglobin, demonstrating improved red blood cell function.”
- Reframing the threshold group as “participants who adhered to the protocol”.
Implies causality the study didn’t test. - Study explicitly reports these as “preliminary associations” and “potentially relevant improvements…warranting further study,” not proven treatment effects.
- These results are part of a non-randomized post-hoc responder exploratory subgroup analysis and are associative only and do not establish causality or clinical efficacy.
Subgroup Charts
Three Group Kruskal–Wallis Test
Study Abstract:
“Half of the participants in the treatment group had a posttreatment C15:0 level >5 μg/mL. In these individuals, there were significantly greater decreases in alanine aminotransferase (−29 U/L, P = 0.001) and aspartate aminotransferase (−6 U/L, P = 0.014), as well as a greater increase in hemoglobin (0.60 g/dL, P = 0.010), as compared with participants that did not reach a posttreatment level >5 μg/mL.”
- P-values come from the three-group Kruskal–Wallis (KW) test
- Three-group KW test only answers: “Are any of the three groups different?”, not which groups differ.
- “as compared with participants that did not reach >5 μg/mL”: reads like a specific two-group comparison (≥5 μg/mL vs <5 μg/mL). The KW test alone does not test that claim.
- You cannot just get a significant KW p-value, look at medians and declare “significantly greater decreases/increases in this group.”
- Would need follow-up two-group test for the exact comparison of interest.
- KW is based on ranks and can reflect differences in spread or tails, not just medians.
- The test is NOT adjusted for baseline levels of the groups.
Clinical Trial 3
List of Metrics unchanged with addition of C15:
Body weight, BMI, Waist circumference, Hip circumference,
Systolic blood pressure, Diastolic blood pressure,
Fasting glucose, Fasting insulin,
Total cholesterol, HDL cholesterol, LDL cholesterol, Triglycerides,
C-reactive protein (CRP), Alanine aminotransferase (ALT), Aspartate aminotransferase (AST), Hemoglobin
Total Metrics measured: 17
Metrics unchanged with fatty15: 16
Metrics changed with fatty15: 1
*it did on average increase C15 levels
Note: in comparison (pre-threshold), GGT was found to be significantly lower in treatment group. In ‘threshold analysis’ it was NOT. Similarly, AST, ALT, Hemoglobin were (at least one group) was different in threshold group analysis, but not in main analysis
Clinical Trial 3: Conflicts of Interest
Seraphina Theraputics was founded by Stephanie Venn-Watson. They make fatty15.
“Among next-step studies is an ongoing double-blinded, placebo-controlled clinical trial with fatty15, which is being independently conducted by Dr. Jeffrey Schwimmer at the University of California, San Diego.” - quote from fatty15 website
Clinical Trial 3 (published 2024)
Conflict of interest: “JBS (Jeffrey Schwimmer) reports grants to UCSD from Intercept and Genfit. All other authors report no conflicts of interest.”
Funding: “The project was also supported by Seraphina Therapeutics including the provision of C15:0 supplements and matching placebo.”
2021 Study from J Clin Invest Conflict of interest:
JBS has received research support from Galmed, Intercept, Genfit, and Seraphina.
2022 UC San Diego News Article: “Disclosure: Jeffrey B. Schwimmer receives grant support from Intercept, Genfit and Seraphina.”
2024 Study from Hepatology Conflicts of interest:
“Jeffrey Schwimmer’s institution received research grants from Genfit, Intercept, and Seraphina”
2025 Study from J Clin Invest Conflict of interest:
JBS reports grant support to the University of California, San Diego, from Seraphina Therapeutics and Thiogenesis Therapeutics.
Fatty15 RCT:
Half didn’t increase C15 levels.
Benefit claims, based on statistical shenanigans, were overstated.
From the 2 actual RCTs on C15:
No replication of minor positive findings
fatty15 on the Skeptics
What the skeptics say
In videos, skeptics go over two clinical trials (Robinson et al. and Chooi et al.) and incorrectly conclude that these trials were not in relevant populations and did not demonstrate efficacy.
Strangely, the skeptics made these statements while showing the papers’ abstracts, where the authors themselves concluded that C15:0 demonstrated promising results.
The skeptics do not mention any of the other five studies and four clinical trials provided above, in part because two are recent publications.
HOW MUCH?
Still want to try fatty15?
- ‘30 day’ means 30 pills, and 100mg per pill.
- Study protocol of 200mg or 300mg
To recreate the study doses:
(based on 90 day subscription)
- $2.67 or $4.00 per day, or $80 or $120 per month
- note: dose > 245mg per day is no longer GRAS
What are you paying for? Marketing!
- “HSA/FSA eligible”
Unsure if you need fatty15?
There’s a $199 test for that!
Fatty15: Another Subscription!
So Many Claims:
“Essential fatty acid” / “past 50 years…population wide declines in C15:0 levels.”
Not supported: C15:0 is not recognized as essential by authorities. No longitudinal population biomarker data proving a decades-long decline. Sources: NIH ODS (EFAs = LA & ALA), Company blog
The 3 authors of the study claiming this are: Founder of fatty15, financed by Epitracker (Venn-Watson owned company), and a scientific advisor to fatty15 who holds equity in the company. Decline over 50 years claim (marketing).“Cellular Fragility Syndrome”
Not supported: Not a recognized medical diagnosis (absent from ICD-11, not a MeSH descriptor). The term is introduced by company-affiliated authors in a single hypothesis/review and amplified in marketing/press; there is no independent clinical validation or diagnostic criteria. See the hypothesis paper (Venn-Watson 2024), company blog (fatty15), and third-party critique (CSPI).Metabolic health (PPAR-α/δ, AMPK, mitochondria)
Not supported in human RCTs: Two 12-week placebo-controlled trials raised circulating C15:0 but showed no improvements in metabolic outcomes (weight, glucose, insulin resistance, triglycerides, blood pressure). Sources: J Nutr RCT (2024)Heart health (LDL; cardiometabolic risk/events)
not supported/insufficient: No trials show fewer CVD events; observational meta-analysis shows no association with all-cause mortality and non-significant pooled associations for some CVD subtypes for 15:0. 12-wk placebo-controlled trial raised blood C15:0 but no between-group improvements in clinical endpoints except small LDL decrease (1/37) (not replicated in other RCT). Sources: PLOS Med meta-analysis (2021)Liver health (enzymes; fatty liver)
Not supported (human): 12 week human RCT trial showed no difference in liver Fat, or liver enzymes. Other lower GGT, (but not in subgroup, lower ALT/AST in subgroup). Unclear/non-replicated results. Sources: J Nutr RCT, AJCN TANGO RCT (2024)Red blood cells (membranes; hemoglobin)
Not Supported (human ITT): Hemoglobin increase seen only in NON-RANDOM subgroup defined after the fact, not vs placebo.
Source: J Nutr RCTImmune health / inflammation (cytokines, CRP)
Not supported (human): No human RCT showing reductions; both human RCTs showed no difference in CRP in C15 group.Cognitive & mental health (dopamine/PPAR; mood/stress)
Insufficient (human): No human trials located; claims are marketing. RCT they claim supports this (not RCT, secondary anlaysis of RCT), authors state “The present study cannot conclude that the group receiving C+15:0 together with the MD had effects in decreasing symptoms.” Example claim: Company blog
So Many Claims:
Sleep quality
Not supported (human): No C15:0 sleep RCTs; “deeper sleep” appears in marketing/surveys. RCT found no difference in sleep duration. Example claim: Product pageHunger/satiety (PPAR-α)
Not supported (human): No RCTs measuring appetite/energy intake/GLP-1/ghrelin.
Example claim: Company postJoint comfort
Not supported (human): No human RCTs on joint pain/function.
Example claim: Marketing copyGut microbiome
Limited/neutral (human): In NAFLD (TABGO) trial, Bifidobacterium adolescentis increase reported with C15:0, but no broader microbiome “health” or clinical GI benefits established.
Source: AJCN TANGO RCTAnti-aging / “slows and reverses aging”
Not supported (human outcomes): No RCTs on aging endpoints or epigenetic clocks; mortality association for 15:0 is null in meta-analysis.
Sources: PLOS Med meta-analysis, Homepage claim, “Reversing cellular aging” blog“Reduces mTOR” (longevity mechanism)
Not supported (human): Based on mechanistic/cell work, not human outcomes.
Sources: Company mTOR blog, Review asserting AMPK↑/mTOR↓ is written by author and of questionable relevance.“3× more cellular benefits than EPA (omega-3)” / “take fatty15 instead of omega-3”
Not supported (human); potentially misleading—arguably borderline unethical. The “3×” figure comes incorrect math from a single in-vitro screen by company-affiliated authors; there are NO human RCTs or animal RCTs showing clinical superiority over EPA. Substitution messaging (implying you should take fatty15 instead of omega-3) conflicts with established recommendations that EPA/DHA remain important nutrients. Comparative health claims promoting substitution away from EPA/DHA conflicts with consensus guidance and, without competent and reliable human evidence, should be backed by competent and reliable scientific evidence, typically well-controlled human trials—which is not present here, a concern under FTC health-claims standards.
Sources: Company claim, FTC Health Products Compliance Guidance, NIH ODS: Omega-3, AHA: Fish & omega-3
Note: This is a scientific/consumer-protection opinion, not legal advice or an allegation of unlawful conduct.
Conclusion
In my view:
- Some observational studies suggest C15:0 may be beneficial, but others are null (no clear association).
- No human RCT evidence supplementation is worth taking
- Impossible to decouple the business and science
- Marketing is borderline harmful and potentially false advertising
- Marketing reads like parody or satire